Cyanide is a highly reactive nucleophile that is common in the environment and is considered a potent suicide, murder and genocide. The notoriety of cyanide has been known to humanity since ancient times. There are many sources of industrial and dietary exposure to cyanide. However, the
most significant source of exposure is the inhalation of smoke in fires in industrial, residential or other random fires. Cyanide is a mitochondrial toxin that affects cellular respiration and causes morbidity or mortality within a short time. It is predominantly a neurotoxin whose toxicity is mediated by the inhibition of cytochrome oxidase, a mitochondrial end-chain enzyme. The effects of cyanide are complex and can not be attributed solely to the lack of oxygen in the cell. Recent mechanistic studies show that cyanide inhibits several enzymes and modifies several important intracellular processes leading to a cascade of toxic events. The treatment of cyanide poisoning should be initiated immediately and aggressively. There are many antidotes to cyanide poisoning, but methemoglobin inducers such as amyl nitrite and / or sodium nitrite in combination with a sulfur donor such as sodium thiosulfate are the most common treatment for cyanide poisoning. Many of the cyanide antidotes are not free from side effects. Therefore, newer molecules are still being studied for cyanide antagonism. In the recent past, many mechanistic-based antidotes have been evaluated. This chapter reviews the established concepts and recent advances in the toxicology of cyanide and its treatments.
Cyanide causes intracellular hypoxia by reversibly binding to mitochondrial cytochrome oxidase a (3). Signs and symptoms of cyanide poisoning usually occur less than 1 minute after inhalation and within minutes of ingestion. Early manifestations include anxiety, headache, dizziness, inability to focus the eyes and mydriasis. As hypoxia progresses, lower levels of consciousness, seizures and coma can progressively occur. The skin may look normal or slightly ashen and the arterial oxygen saturation may be normal. Early respiratory signs include transient rapid and deep breathing. As poisoning progresses, the hemodynamic status may become unstable. The key treatment is the early administration of one of the two antidotes currently available in the US: the well-known cyanide antidote kit and hydroxocobalamin. Hydroxocobalamin detoxifies cyanide by binding to it, producing the renally excreted non-toxic cyanocobalamin. Hydroxocobalamin binds with cyanide without forming methemoglobin and can therefore be used to treat patients without compromising the oxygen transport capacity of hemoglobin. FEWER
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